Growth hormone plus resistance exercise attenuate structural changes in rat myotendinous junctions resulting from chronic unloading

Its about atrophy so your doctor needs to use this knowledge to prevent it from happening to stroke patients. Abstract first and then a couple of iteresting paragraphs.

Growth hormone plus resistance exercise attenuate structural changes in rat myotendinous junctions resulting from chronic unloading

Abstract

Myotendinous junctions (MTJs) are specialized sites on the muscle surface where forces
generated by myofibrils are transmitted across the sarcolemma to the extracellular matrix. At
the ultrastructural level, the interface between the sarcolemma and extracellular matrix is
highly folded and interdigitated at these junctions.
 
In this study, the effect of exercise and growth hormone (GH) treatments on the
changes in MTJ structure that occur during muscle unloading, has been analyzed. Twenty
hypophysectomized rats were assigned randomly to one of five groups: ambulatory control,
hindlimb unloaded, hindlimb unloaded plus exercise (3 daily bouts of 10 climbs up a
ladder with 50% body wt attached to the tail), hindlimb unloaded plus GH (2 daily injections
of 1 mg/kg body wt, i.p.), and hindlimb unloaded plus exercise plus GH. MTJs of the
plantaris muscle were analyzed by electron microscopy and the contact between muscle
and tendon was evaluated using an IL/B ratio, where B is the base and IL is the interface
length of MTJ’s digit-like processes. After 10 days of unloading, the mean IL/B ratio was significantly lower in unloaded (3.92), unloaded plus exercise (4.18), and unloaded plus GH
(5.25) groups than in the ambulatory control(6.39) group. On the opposite, the mean IL/B
ratio in the group treated with both exercise and GH (7.3) was similar to control. These
findings indicate that the interaction between exercise and GH treatments attenuates the
changes in MTJ structure that result from chronic unloading and thus can be used as a
countermeasure to these adaptations.
end of abstract. 

Increased muscle use can also protect muscle mass during muscle wasting conditions
that are associated with stroke, sepsis, cancer, and AIDS. Exercise training alone or combined
with nutritional supplementation has been shown to induce skeletal muscle hypertrophy,
thus aiding rehabilitation or reducing muscle wasting.18,19 During rehabilitation, exerciseinduced
myogenesis may be in part responsible for the recovery of muscle mass.20 Several
interventions aimed to slow or prevent muscle mass loss during periods of disuse have been
explored, indicating that either intermittent muscle training or pharmacological treatments
could slow atrophy. For example, a combination of daily resistance exercise and GH treatment
was capable of maintaining nearly all of the myofibrillar protein content, increasing
protein synthesis in the gastrocnemius of hind-limb unloaded rats.21
In the current investigation, we test the hypothesis that loss of MTJ structural complexity
that occurs during reduced muscle loading can be attenuated by GH treatments or intermittent
exercise. We also propose that combined administration of GH with intermittent
exercise have an additive effect on protecting MTJ structure. Finally, we compare the protective
effects of GH treatments and exercise on MTJ structure with their influences on muscle
mass, to assess whether similar regulatory processes are involved in maintaining MTJ
structure and muscle mass